FUNCTIONAL-SIGNIFICANCE AND CONTROL OF RELEASE OF PULMONARY SURFACTANT IN THE LIZARD LUNG

Citation
Pg. Wood et al., FUNCTIONAL-SIGNIFICANCE AND CONTROL OF RELEASE OF PULMONARY SURFACTANT IN THE LIZARD LUNG, American journal of physiology. Regulatory, integrative and comparative physiology, 38(4), 1995, pp. 838-847
Citations number
31
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
38
Issue
4
Year of publication
1995
Pages
838 - 847
Database
ISI
SICI code
0363-6119(1995)38:4<838:FACORO>2.0.ZU;2-H
Abstract
The amount of pulmonary surfactant in the lungs of the bearded dragon (Pogona vitticeps) increases with increasing body temperature. This in crease coincides with a decrease in lung compliance. The relationship between surfactant and lung compliance and the principal stimuli for s urfactant release and composition (temperature, ventilatory pattern, a nd autonomic neurotransmitters) were investigated. We chose to investi gate ventilatory pattern (which causes mechanical deformation of the t ype II cells) and adrenergic agents, because they are the major stimul i for surfactant release in mammals. To examine the effects of body te mperature and ventilatory pattern, isolated lungs were ventilated at e ither 18 or 37 degrees C at different ventilatory regimens. An isolate d perfused lung preparation at 27 degrees C was used to analyze the ef fects of autonomic neurotransmitters. Ventilatory pattern did not affe ct surfactant release, composition, or lung compliance at either 18 or 37 degrees C. An increase in temperature increased phospholipid reupt ake and disproportionately increased cholesterol degradation/uptake. E pinephrine and acetylcholine stimulated phospholipid but not cholester ol release. Removal of surfactant caused a decrease in compliance, reg ardless of the experimental temperature. Temperature appears to be the principal determinant of lung compliance in the bearded dragon, actin g directly to increase the tone of the smooth muscle. Increasing the a mbient temperature may result in greater surfactant turnover by increa sing cholesterol reuptake/degradation directly and by increasing circu lating epinephrine, thereby indirectly increasing phospholipid secreti on. We suggest that changing ventilatory pattern may be inadequate as a mechanism for maintaining surfactant homeostasis, given the disconti nuous, highly variable reptilian breathing pattern.